This editorial refers to ‘Inhibition of rupture of established atherosclerotic plaques by treatment with apolipoprotein A-I’ by G.J. Reimers et al. , doi:10.1093/cvr/cvr057 Association studies and epidemiological observations have shown that high plasma levels of high-density lipoprotein-cholesterol (HDL-C) provide cardiovascular protection.1 The anti-atherosclerosis activity of HDL is multifaceted and may include anti-thrombotic, anti-oxidative, and anti-inflammatory mechanisms. However, reverse cholesterol transport through which cholesterol is removed from tissues and plaques and shuttled to the liver for excretion with bile is thought to be the major action of HDL in its atheroma-preventing effort. These observations and experimental findings gave rise to studies in experimental animals and phase I and II trials of short-term infusions of reconstituted HDL with the aim of accelerating reverse cholesterol transport.2–4 In the ERASE clinical trial reconstituted HDL (made of human apolipoprotein A-1, Apo A-1, and soybean phosphatidylcholine) that was administered beginning shortly after an acute coronary syndrome tended to reduce …